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Objective To explore the efficacy of triple therapy and sequential therapy in the eradication of Helicobacter pylori (Hp) in patients receiving long-term non-steroidal antiinflammatory drugs (NSAID) treatment.Methods Patients receiving long-term NSAID treatment were enrolled in this study.Patients diagnosed as Hp infection were divided into triple therapy and sequential therapy groups.The patients in triple therapy group received omeprazole,clarithromycin and amoxicillin theray for 10 days.The patients in sequential group received esomeprazole with amoxicillin for five days,and then esomeprazole with clarithromycin and metronidazole for another five days.All patients were given mucosal protective therapy as maintenance treatment after eradication therapy and followed up for 12 weeks.Patients underwent endoscopy examination and Hp testing before and after follow-up.Hp eradication rates were compared with the intention-to-treat (ITT) and per protocol (PP) analysis.Results According to ITT analysis,the eradication rates of Hp in triple therapy group and sequential therapy group were 78.4 ％ (40/51) and 80.0 ％ (40/50) respectively,there was no significant difference between these two groups (x2 =0.038,P=0.846).According to PP analysis,the eradication rates of Hp in triple therapy group and sequential therapy group were 84.4％ (38/45) and 87.0％ (40/46) respectively,there was no significant difference between these two groups either (x2=0.117,P=0.732).Conclusion There was no significant difference in Hp eradication between triple therapy and sequential therapy in patients receiving long-term NSAID treatment.
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Objective To investigate the prevalence and the risk factors of gastroduodenal damages induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Methods One hundred and eighty-four patients who were prescribed NSA1Ds for long time in rheumatology and cardiovascular clinics were enrolled. Clinical data such as age, sex, medication history and body mass index were recorded. The lesions were estimated by endoscopy and the specimens were tested for Helicobacter pylori (H. pylori) infection. Results Peptic ulcer was found in 63 (34. 24%) patients including gastric ulcer in 22, duodenal ulcer in 34 and compound ulcer in 7. The endoscopic examination showed that 57 out of 121 patients without peptic ulcer had ≥3 erosive lesions. Logistic regression analysis revealed that H. pylori infection was important risk factor that induced the peptic ulcer in those who were taking NSAIDs for long time (OR = 13. 86, 95% CI: 6. 53 ～ 29. 43). The incidence of gastroduodenal damage was similar in patients taking NSAIDs and low dose aspirin (OR =0.45,95CI:0.16～ 1.28). Conclusions NSAIDs may cause gastroduodenal damages in long-term users and H. pylori infection was an important risk factor. The effect of low dose aspirin on gastroduodenal damages is as same as NSAIDs.
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Objective To investigate inhibitory effect of Telmisartan on carotid arterial intima-media thickness in patients with essential hypertension. Methods 104 patients with mild or mid essential hypertension were randomly divided into three groups, which include telmisartan group( telmisartan 80 mg/d PO), ramipril group( ramipril 5 mg/d PO), and control group( other anti-hypertension agents). Blood pressure was monitored during treatment. Carotid arterial intima-media thickness(CIMT) were measured in all patients at beginning and patients who had the 12 months course. Results There were 91 patients who had the 12 months course,which include telmisartan group33 cases,ramipril group28 cases, and control 30 cases. The CIMT was significantly decreased in telmisartan group and ramipril group ( all P < 0. 05 ), and not changed in control while blood pressure fall effectively. In ramipril, group5 cases were ceased the course because of severe cough. Conclusion Both telmisartan and ramipril could decrease blood pressure and CIMT effectively, and there were less side effects in telmisartan group.
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0.05) for penetrating blood vessel, 46% and 18%( P
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OBJECTIVE: To evaluate the efficacy and safety of Pravastatin versus Simvastatin in downregulating low density lipoprotein cholesterol(LDL-C) and upregulating high density lipoprotein cholesterol(HDL-C).METHODS: A total of 66 patients with hypercholesterolemia were enrolled: 33 were randomly assigned to receive Pravastatin(40 mg) for 6 weeks,and another 33 to receive Simvastatin(40 mg) for 6 weeks.Serum lipid levels at baseline and 6 weeks after medication were measured.The primary effective indicator was LDL-C as compared with baseline value and the secondary effective indicator was HDL-C.Safety was evaluated based on laboratory data and clinical adverse reactions.RESULTS: Both Pravastatin and Simvastatin significantly decreased LDL-C level,showing significant differences as compared with before medication(P0.05).Less adverse drug reactions were noted in both groups.CONCLUSION: Pravastatin and Simvastatin were equivalent in lipid-regulatory effect and both were well-tolerated.
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60 mmHg), indicating that the increase in pulse pressure participates in the course of myocardial hypertrophy. ⑤There was no significant correlation between pulse pressure and serum IGF-1 concentra tion, suggesting that different mechanisms are involved in the development of my ocardial hypertrophy between pulse pressure and IGF-1.